About

Yang Dan is a Professor of Neuroscience and a Howard Hughes Medical Investigator at the University of California, Berkeley. She holds the Chancellor's Chair in Neuroscience and is part of the Pivotal Life Sciences division. Her research focuses on neural circuits controlling sleep and the mechanisms of executive control. As a faculty member, she is involved in advancing understanding of these complex neural processes, contributing to the broader field of neuroscience through her research and academic leadership.

Research topics

• Computer Science
• Neuroscience
• Psychology
• Cognitive psychology
• Medicine
• Statistics
• Pathology

Selected publications

• Activation of locus coeruleus noradrenergic neurons rapidly drives homeostatic sleep pressure

  Science Advances · 2025-01-17 · 24 citations

  articleOpen accessSenior authorCorresponding

  Homeostatic sleep regulation is essential for optimizing the amount and timing of sleep for its revitalizing function, but the mechanism underlying sleep homeostasis remains poorly understood. Here, we show that optogenetic activation of locus coeruleus (LC) noradrenergic neurons immediately increased sleep propensity following a transient wakefulness, contrasting with many other arousal-promoting neurons whose activation induces sustained wakefulness. Fiber photometry showed that repeated optogenetic or sensory stimulation caused a rapid reduction of calcium activity in LC neurons and steep declines in noradrenaline/norepinephrine (NE) release in both the LC and medial prefrontal cortex (mPFC). Knockdown of α 2 A adrenergic receptors in LC neurons mitigated the decline of NE release induced by repetitive stimulation and extended wakefulness, demonstrating an important role of α 2 A receptor–mediated auto-suppression of NE release. Together, these results suggest that functional fatigue of LC noradrenergic neurons, which reduces their wake-promoting capacity, contributes to sleep pressure.

  PublisherDOI

• Neuroendocrine circuit for sleep-dependent growth hormone release

  Cell · 2025-06-24 · 11 citations

  articleOpen accessSenior author

  Sleep is known to promote tissue growth and regulate metabolism, partly by enhancing growth hormone (GH) release, but the underlying circuit mechanism is unknown. We demonstrate how GH release, which is enhanced during both rapid eye movement (REM) and non-REM (NREM) sleep, is regulated by sleep-wake-dependent activity of distinct hypothalamic neurons expressing GH-releasing hormone (GHRH) and somatostatin (SST). SST neurons in the arcuate nucleus suppress GH release by inhibiting nearby GHRH neurons that stimulate GH release, whereas periventricular SST neurons inhibit GH release by projecting to the median eminence. GH release is associated with strong surges of both GHRH and SST activity during REM sleep but moderately increased GHRH and decreased SST activity during NREM sleep. Furthermore, we identified a negative feedback pathway in which GH enhances the excitability of locus coeruleus neurons and increases wakefulness. These results elucidate a circuit mechanism underlying bidirectional interactions between sleep and hormone regulation.

  PublisherOA PDFDOI

• A common computational and neural anomaly across mouse models of autism

  Nature Neuroscience · 2025-06-03 · 4 citations

  articleOpen access
  PublisherOA PDFDOI

• The how and why of sleep: Motor theory and catecholamine hypothesis

  Neuron · 2025-09-16 · 4 citations

  reviewOpen accessSenior author

  Sleep entails profound changes in the brain and body, marked by altered states of consciousness and reduced somatic and autonomic motor activity. Regarding "how" sleep is regulated, whole-brain screening revealed large sleep-control networks spanning the forebrain, midbrain, and hindbrain. We unify diverse experimental evidence under a "motor theory," in which the sleep-control mechanism is integral to somatic and autonomic motor circuits. Regarding the "why" question, sleep deprivation impairs cognition, emotion, metabolism, and immunity. We propose catecholamine (dopamine, noradrenaline, and adrenaline) inactivation as the fundamental biological process underlying sleep's numerous benefits. Beyond brain arousal and motor activity, catecholamines regulate metabolism and immunity; their sleep-dependent suppression yields wide-ranging advantages, promoting repair and rejuvenation. Furthermore, catecholaminergic neurons are metabolically vulnerable; their need for rest and recovery may drive homeostatic sleep pressure. Together, the motor theory offers a unifying framework for sleep control, while the catecholamine hypothesis posits a core mechanism mediating sleep's multifaceted benefits.

  PublisherDOI

• Brainstem circuit for sickness-induced sleep

  Science Advances · 2025-12-10 · 2 citations

  articleOpen accessSenior author

  Increased sleep induced by immune activation plays a crucial role in facilitating recovery from illness. However, the neural mechanisms underlying sickness-induced sleep remain poorly understood. Here, we identify a brainstem circuit originating in the nucleus of the solitary tract (NST) that mediates sickness-induced nonrapid eye movement (NREM) sleep. Using activity-dependent genetic labeling, we tagged NST neurons activated by lipopolysaccharide (LPS) injection and showed that their chemogenetic activation strongly promotes NREM sleep. These NST neurons project extensively to the parabrachial nucleus (PB), where LPS-activated neurons also promote NREM sleep. Fiber photometry recording of several wake-promoting neuromodulators using their biosensors showed that evoked norepinephrine release from locus coeruleus neurons is markedly reduced by either LPS injection or direct activation of NST or PB sickness neurons. These results suggest that sickness-induced NREM sleep is mediated in part by a brainstem circuit that regulates neuromodulator signaling.

  PublisherDOI

• Brain-wide representations of prior information in mouse decision-making

  Nature · 2025-09-03 · 43 citations

  articleOpen access

  . Here, to investigate them, we examined brain-wide Neuropixels recordings and widefield calcium imaging collected by the International Brain Laboratory. Mice were trained to indicate the location of a visual grating stimulus, which appeared on the left or right with a prior probability alternating between 0.2 and 0.8 in blocks of variable length. We found that mice estimate this prior probability and thereby improve their decision accuracy. Furthermore, we report that this subjective prior is encoded in at least 20% to 30% of brain regions that, notably, span all levels of processing, from early sensory areas (the lateral geniculate nucleus and primary visual cortex) to motor regions (secondary and primary motor cortex and gigantocellular reticular nucleus) and high-level cortical regions (the dorsal anterior cingulate area and ventrolateral orbitofrontal cortex). This widespread representation of the prior is consistent with a neural model of Bayesian inference involving loops between areas, as opposed to a model in which the prior is incorporated only in decision-making areas. This study offers a brain-wide perspective on prior encoding at cellular resolution, underscoring the importance of using large-scale recordings on a single standardized task.

  PublisherOA PDFDOI

• A brain-wide map of neural activity during complex behaviour

  Nature · 2025-09-03 · 61 citations

  articleOpen access

  . It is difficult to meet this challenge if different laboratories apply different analyses to different recordings in different regions during different behaviours. Here we report a comprehensive set of recordings from 621,733 neurons recorded with 699 Neuropixels probes across 139 mice in 12 laboratories. The data were obtained from mice performing a decision-making task with sensory, motor and cognitive components. The probes covered 279 brain areas in the left forebrain and midbrain and the right hindbrain and cerebellum. We provide an initial appraisal of this brain-wide map and assess how neural activity encodes key task variables. Representations of visual stimuli transiently appeared in classical visual areas after stimulus onset and then spread to ramp-like activity in a collection of midbrain and hindbrain regions that also encoded choices. Neural responses correlated with impending motor action almost everywhere in the brain. Responses to reward delivery and consumption were also widespread. This publicly available dataset represents a resource for understanding how computations distributed across and within brain areas drive behaviour.

  PublisherOA PDFDOI

• Lightning Pose: improved animal pose estimation via semi-supervised learning, Bayesian ensembling and cloud-native open-source tools

  Nature Methods · 2024-06-25 · 57 citations

  articleOpen access
  PublisherOA PDFDOI

• The How and Why of Sleep: Motor Theory and Catecholamine Hypothesis

  2024-01-19

  preprintOpen accessSenior author

  The transition from wakefulness to sleep is associated with profound changes in the brain and body. In addition to altered states of consciousness, there are marked reductions in somatic and autonomic motor activity. To understand how mammalian sleep is generated, whole-brain screening for sleep neurons has revealed a large network spanning the forebrain, midbrain, and hindbrain. We unify various experimental findings in a “motor theory”, in which the sleep-control mechanism is integral to somatic and autonomic motor control circuits, allowing coordinated reductions in mental arousal and physical activity for sleep generation. Regarding the why question, sleep deprivation is known to cause metabolic and immune disruptions in addition to cognitive and emotional impairments, but could these diverse effects be traced to a single, basic biological process? We here propose a “catecholamine hypothesis”, in which inactivation of catecholamine (dopamine, noradrenaline and adrenaline) signaling is essential for not only sleep generation but also the various benefits of sleep. Besides promoting brain arousal and somatic/autonomic motor activity, catecholamines are master regulators of metabolic and immune functions; suppression of catecholamine activity during sleep has wide-ranging effects that together facilitate repair and rejuvenation. Furthermore, catecholaminergic neurons are particularly vulnerable to metabolic stress and neurodegeneration. Such vulnerability, hence the recurring need for rest and recovery of these neurons, may be a major cause for homeostatic sleep pressure. Thus, the motor theory offers a simple framework for understanding how sleep is controlled by a distributed circuit mechanism, and the catecholamine hypothesis posits a singular process that underpins the multifaceted reasons for sleep.

  PublisherOA PDFDOI

• A brainstem maestro conducting the somatic and autonomic motor symphony

  Cell · 2024-06-01 · 1 citations

  articleOpen accessSenior authorCorresponding
  PublisherOA PDFDOI

Recent grants

• Clonal origin of visual cortical microcircuitry

  NIH · $3.0M · 2008–2017

• NIH Grant R01EY014887

  NIH · $1.4M · 2007

• NIH Grant R01EY015180

  NIH · $1.2M · 2009

• NIH Grant R01EY012561

  NIH · $1.1M · 2006

Frequent coauthors

• Mu‐ming Poo

  Shanghai Institutes for Biological Sciences

  60 shared

• Chenyan Ma

  34 shared

• Danqian Liu

  29 shared

• Siyu Zhang

  Huaqiao University

  26 shared

• Min Xu

  Wuxi People's Hospital

  25 shared

• Peng Zhong

  Shanghai Jiao Tong University

  24 shared

• Shinjae Chung

  University of Pennsylvania

  21 shared

• Wei-Cheng Chang

  University of California, Berkeley

  21 shared

Education

• PhD, Biological Sciences

  Columbia University

  1994

• BS, Physics

  Peking University

  1988

Awards & honors

• Howard Hughes Medical Investigator
• Chancellor's Chair in Neuroscience